Article Publish Status: FREE
Abstract Title:

Resveratrol ameliorates brain injury via the TGF-β-mediated ERK signaling pathway in a rat model of cerebral hemorrhage.

Abstract Source:

Exp Ther Med. 2019 Nov ;18(5):3397-3404. Epub 2019 Aug 26. PMID: 31602214

Abstract Author(s):

Riguang Zhao, Kun Zhao, Hongjun Su, Peng Zhang, Na Zhao

Article Affiliation:

Riguang Zhao


Brain injury is the most common intracranial injury in human cerebrovascular disease, which may lead to ischemic stroke. Resveratrol induces ameliorative effects in the treatment of certain human diseases by regulating different signaling pathways. The present study assessed the therapeutic effects of resveratrol and its potential mechanism of action in the neurons from rats with ischemia/reperfusion-induced cerebral hemorrhage. The rat model of cerebral hemorrhage was established and reverse transcription-quantitative polymerase chain reaction, western blotting, immunohistochemistry and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays were subsequently performed to assess the therapeutic effects of resveratrol. The results demonstrated that treatment with resveratrol (10 mg/kg/day) decreased cerebral water content, hippocampal cell apoptosis and cerebral infarct volume compared with the PBS-treated group. Resveratrol treatment also increased neuronal cell viability, improved neurological function and blood brain barrier disruption compared with the PBS group following 21 days of treatment. The administration of resveratrol was demonstrated to decrease the levels of certain inflammatory factors, including ionized calcium binding adaptor molecule 1 and myeloperoxidase, in rats with cerebral hemorrhage. The results revealed that treatment with resveratrol regulated neuronal apoptosis by downregulating the transforming growth factor-β (TGF-β)-mediated extracellular signal-regulated kinase (ERK) signaling pathway. In conclusion, these results indicate that resveratrol decreases ischemia/reperfusion-induced neuronal apoptosis by downregulating the TGF-β-mediated ERK pathway in a rat model of cerebral hemorrhage and may serve as a potential agent for the treatment of cerebral hemorrhage.

Study Type : Animal Study

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